The transition of bacterial cells from planktonic to biofilm form is induced by the regulation of gene expression in response to sensed physicochemical environmental signals such as ions, pH, and nutrients, which in turn affects various signaling pathways 3. Biofilm infections are highly resistant to antibiotic therapy and host defense, making biofilms difficult to be eradicated 2. Biofilm-related infections occupy a large percentage of nosocomial infections 1, including device and indwelling catheter infections. An intervention to target glutamate intake may be a potential useful approach against biofilm.īiofilms are aggregates of bacteria that are adherent to a material surface and encased in a self-synthetic extracellular polymer matrix. In conclusion, we showed that gltS was a critical regulator of biofilm formation by controlling the intake of exogenous glutamate. We also showed that urea cycle activation was critical for biofilm formation. The deficiency of exogenous glutamate intake accelerated endogenous glutamate/glutamine production, which led to the activation of the urea cycle. The lack of exogenous glutamate also enhanced biofilm formation in JE2 strain. This was shown by gltS transposon mutant as well as its complementation. Here we examined the role of ion transporters in biofilm formation and found that the sodium-glutamate transporter gltS played an important role in biofilm formation in MRSA. Although biofilm is induced by a number of environmental signals, the molecule responsible for environmental sensing is not well delineated. Methicillin-resistant Staphylococcus aureus (MRSA) is one of major organisms responsible for biofilm infection. Biofilm-based infection is a major healthcare burden.
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